24 Flashcards
Management of child with altered mental status
Management of the Child With Altered Mental Status
CABs
When a child presents with altered mental status—or any potentially serious illness—you must first assess the patient’s circulation, airway, and breathing. Your goal is to identify any life-threatening conditions and avoid further deterioration. Many EDs will check a fingerstick blood glucose on arrival of an unresponsive child.
Gathering Information
After determining from the vital signs that the patient is stable, you should then gather more historical information, perform a more detailed exam, and order appropriate tests.
Ordering Studies
Depending on the initial differential diagnosis in mind you would also consider ordering a toxicology screen and a CT scan of the head and possibly doing a lumbar puncture, but again, all of these would happen after initial assessment of CABs.
Tx of hypoglycemia, hypotension and tachycardia 3
Treatment of Hypoglycemia, Hypotension, and Tachycardia
Immediate treatment to address hypoglycemia, hypotension, and tachycardia would include giving boluses of 20cc/kg normal saline and 25% dextrose. These can be followed by administration of fluids with 10% dextrose at maintenance.
It is critical to rapidly correct the hypoglycemia and frequently reassess both the blood sugar and the blood pressure to make sure the child is responding to the therapy.
Very acute onset of altered mental status in a toddler should raise a concern for
Ingestion/ toxin exposure
Drug class and clinical features (toxidrome) 5
Cholinergic
(organophosphates)
Miosis and blurred vision
Increased gastric motility (nausea, vomiting, diarrhea)
Excessive tearing, salivation, sweating and urination
Bronchorrhea and bronchospasm
Muscle twitching and weakness
Bradycardia
Seizures and coma
Mnemonic:DUMBBELS- diarrhea, urination, miosis, bradycardia, bronchoconstriction, emesis, lacrimation, salivation
Anticholinergic
(diphenhydramine, tricyclic antidepressants)
Mydriasis (dilated pupils) "blind as a bat" Dry skin "dry as a bone" Red skin (flushed) "red as a beet" Fever "hot as Hades" Delirium and seizures "mad as a hatter" Tachycardia Urinary retention Ileus
Sedative-hypnotic
(benzodiazepines, barbiturates)
Blurred vision (miosis or mydriasis) Hypotension Apnea and bradycardia Hypothermia Sedation, confusion, delirium, coma
Opioids
(codeine, morphine, heroin) Miosis (constricted pupils) Respiratory depression Bradycardia and hypotension Hypothermia Depressed mental status (sedation, confusion, coma)
Sympathomimetics
(cocaine, amphetamines, pseudoephedrine)
Mydriasis
Fever and diaphoresis
Tachycardia
Agitation and seizures
Diff dx of ingestion causing altered mental status and mydriasis 9
Tricyclic antidepressant
Agitation, cardiac manifestations (especially hypotension), dilated pupils and dry, hot skin are classic findings in TCA ingestions.
Clinical findings would vary with dose.
In a 2-year-old, ingestion of only one to two pills of nortriptyline can cause serious symptoms.
Selective serotonin reuptake inhibitor
An ingestion of an SSRI antidepressant requires a significant overdose to cause toxicity.
These overdoses cause a serotonin syndrome (profuse sweaty skin, agitation, fever, mental status changes, diarrhea, myoclonus, hyperreflexia, ataxia, and shivering).
Antihistamine
Antihistamine ingestions present with anticholinergic effects much like those in TCA ingestions, though TCA ingestions have additional mechanisms that cause unique cardiac manifestations.
Decongestant
An overdose of a decongestant results in a sympathomimetic toxidrome.
This presents with tachycardia and hypertension, as well as agitation, sweating, fever, mydriasis and seizures.
Iron
Presents with severe abdominal symptoms followed by signs of shock.
Beta-blocker
Causes bradycardia.
Acetaminophen
Initially presents with minimal symptoms (though gastrointestinal symptoms are not uncommon) followed by symptoms of liver toxicity.
Aspirin
Presents with agitation and tachycardia but there is no mydriasis.
Opioid
Causes sedation and constricted pupils (miosis).
Mech of TCA toxicity
Sxs
The mechanism of tricyclic toxicity is complex.
TCAs have the following effects:
Inhibition of synaptic reuptake of norepinephrine and serotonin
Antagonism of muscarinic acetylcholine receptors and peripheral alpha receptors (normally causes vasoconstriction), and
Blockade of sodium channels and GABA receptors.
Clinically, therefore, patients present with:
Altered mental status
Anticholinergic signs and symptoms
Hypotension (a hallmark of TCA toxicity)
Dysrhythmias, and
Seizures
Hypotension stems from direct myocardial depression from sodium channel blockade, and especially peripheral vasodilatation from alpha-1 adrenergic blockade.
Refractory hypotension is the most common cause of death from TCA overdose.
Evaluation of AMS 7
Glucose
In cases of hypoglycemia, continued monitoring of serum glucose is needed. (If hypoglycemia persists, maintenance dextrose should be provided. Octreotide—a somatostatin analog—inhibits insulin release and may be indicated as an antidote in dextrose-refractory sulfonylurea overdose.)
CBC
A CBC will provide evidence in cases of an infectious etiology.
Electrolytes
Electrolytes and a blood gas can be used to identify metabolic acidosis/anion gap, which would be characteristic of aspirin or NSAID toxicity.
EKG
An EKG is critical to identify possible dysrhythmias.
Calcium
Abnormal levels of calcium can also affect cardiac function.
Toxicology screen
A toxicology screen from the urine or blood should be done to confirm the working diagnosis. Although the results will not be immediately available, it is important to obtain the sample early.
Acetaminophen
Acetaminophen is the most common accidental ingestion. Acetaminophen toxicity initially presents with minimal symptoms.
Decontamination Tx alternatives 4
Physicians opinions differ on whether not to give decontamination after toxic ingestion
Activated charcoal
Indicated for ingestions not due to small molecules or heavy metals.
Contraindicated in a patient with a loss of protective airway reflexes due to the risk of aspiration; selective intubation should be considered in such cases.
Additional doses of activated charcoal may be indicated due to decreased gastrointestinal motility as a result of the anticholinergic effects of tricyclics.
Cathartic agent - accelerates defecation
A single dose of a cathartic agent may be given with the initial dose of charcoal.
Nasogastric lavage Nasogastric lavage has not demonstrated consistent clinical benefit:
One adult study demonstrated improved clinical outcomes within one hour of a tricyclic ingestion.
It would be technically difficult to a pass a large enough tube in a two-year-old child.
Syrup of ipecac
The AAP recommends that syrup of ipecac not be used as first-line therapy for ingestions due to potential side effects.
Syrup of ipecac is contraindicated when there is a risk of aspiration with an altered mental status and the potential for serious cardiac side effects and seizures.
EKG findings in TCA toxicity 4
Cardiotoxicity is primarily responsible for most of the morbidity and mortality seen in TCA overdose. Typical EKG findings include:
Irregularly irregular rhythm
P waves not distinctly seen and increased PR interval
Widened QRS (slower spread of ventricular depolarization)
Prolonged QT interval
Sodium channel blockade affects the His-Purkinje conduction system as well as myocardial cells
A wide-complex tachycardia is the characteristic life-threatening dysrhythmia seen with severe TCA toxicity. The wide-complex tachycardia seen with TCA toxicity, however, is often not ventricular tachycardia, but sinus tachycardia with a wide QRS / aberrant conduction. A slow, wide-QRS idioventricular rhythm is usually pre-terminal.
Management of TCA toxicity Cardiac monitoring Mainstay tx Anti arrhythmics Tx of hypotension Tx of seizures
Suspicion of tricyclic antidepressant toxicity requires immediate evaluation and treatment, since toxicity can progress rapidly. The management of the patient with a TCA ingestion depends on clinical presentation.
Cardiac Monitoring
Continuous cardiac monitoring and serial EKG’s are required for a minimum of 6 hours.
Most patients develop major clinical toxicity within several hours of presentation.
Duration of monitoring depends on many factors.
Serum Alkalization
The mainstay treatment for cardiotoxicity (triad = conduction delays, dysrhythmias, and hypotension) is serum alkalization and sodium loading. It is indicated for the following:
QRS > 100 msec R wave in AVR > 3mm Wide-complex tachycardias Fluid-refractory hypotension Seizures The serum pH affects protein binding of TCAs, and metabolic acidosis can depress cardiac function.
Dose and Frequency
Hypertonic sodium bicarbonate is given as a 1 mEq/kg bolus initially and every three to five minutes until the QRS narrows and hypotension improves. Serum alkalization is continued for 12-24 hours after the EKG normalizes because of the drug’s redistribution from the tissues.
Target pH
The target serum pH is 7.50-7.55, and close monitoring of blood gases is required.
Antiarrhythmics
For life-threatening dysrhythmias, lidocaine can be administered.
Class IA antiarrhythmic drugs, which are sodium channel blockers, are contraindicated.
Class III antiarrhythmic drugs (which can prolong the QT interval) may also be contraindicated.
Treatment of Hypotension
For hypotension, volume expansion, and serum alkalization and sodium loading are the mainstays of therapy, while norepinephrine may be used in refractory situations (0.1-0.2 mcg/kg/min).
Beta-adrenergic agonists and dopamine are contraindicated.
Treatment of Seizures
Seizures are generally brief. In addition to alkalinization, benzodiazepines, barbiturates or propofol may be used.
Phenytoin use is controversial and is usually not indicated due to its potential for cardiac toxicity.
